Having HORs—and that is a frequently heard objection against such theories—would require the ability to refer to oneself. And this, in turn, seems to entail the possession of some notion of the self, the representation of oneself to which other representational states can be bound. As mentioned above, it is typical for noncompetitive NMDA antagonists like ketamine and phency-clidine to cause bizarre ego disorders. Patients report what has been called an ego dissolution, a loosening of the ego boundaries that may end up in a feeling of merging with the cosmos, and an ego disintegration, i.e., a loss of control over thought processes. Like the anesthetic effects, these psychotomimetic effects of the non-competitive NMDA antagonists are highly correlated with their relative affinity for the NMDA receptor. S(+) ketamine, which has a high affinity, is much more potent than the R(—) enan-tiomer (Vollenweider 1998). It follows that NMDA-dependent processes not only are essential for the occurrence of conscious states as such, but also determine the phenomenal content of these states. In particular, they are responsible for the HOR content that says I am in this very mental state. This is in accordance with the HOR hypothesis, which assumes that firstorder representations must be connected with the representation of the self in order to produce the subjective character of conscious states. If this binding operation is disturbed, it will result in HORs whose phenomenal content seems different.
Psychedelic states can be caused by a variety of drugs. Most of these compounds are analogues of transmitter molecules and act preferentially upon specific synapses. Apart from the noncompetitive NMDA antagonists, four major groups of psychedelics are known that interact with cholinergic, noradrenergic, dopaminergic, or serotonergic synapses. Surprisingly, the psychological effects of these different drugs are very similar. All of them produce a psychosis-like syndrome that shares a number of symptoms with schizophrenia. In particular, all of these compounds produce ego disorders (Vollenweider 1998).
There have been attempts to explain the similarity of symptoms. Vollenweider (1998) has proposed that the disturbances arise from defects of sensory information processing in several cortico-striato-thalamo-cortical feedback loops. He assumes that in these loops cholinergic, nor-adrenergic, dopaminergic, serotonergic, and glu-tamatergic synapses are arranged in series so that pharmacological blockades at different links of the chain have the same outcome.
On the basis of the present hypothesis, however, an alternative explanation for the similarity of psychedelic states can be proposed that joins the pharmacology of psychedelic drugs with a realization theory for altered states of consciousness. The ascending reticular activating system consists—as we now know—of several discrete subsystems, each using a single neuro-transmitter. Cholinergic projections arise in the nucleus basalis of Meynert; dopaminergic, in the ventral tegmental area; noradrenergic, in the locus coeruleus; and serotonergic, in the brain stem raphe nuclei. The cortical projections of all four subsystems are widely distributed, reaching into all cortical areas. It is therefore possible that the similar effects of pharmacological interventions into these different projection systems result from their convergence on a common cortical target, the cortical NMDA receptor.
Thus, the cortical NMDA receptors could be the final common target not only of anesthetics but also of psychedelic drugs. A similar mechanism has been suggested for the psychotic symptoms in schizophrenia (Flohr 1992). According to the present hypothesis, the primary cause of schizophrenic symptoms could be either a malfunction of the cortical NMDA synapses themselves (as stated by the NMDA hypothesis of schizophrenia), or, which is also possible in the account of the present hypothesis, a defect of subcortical systems (as is stated, for instance, by the dopamine hypothesis). In any case, the ultimate common cause of the altered states of consciousness would have to be located at the level of cortical information processing.
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